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ENGLISH ABSTRACT
JOURNAL ARTICLE
[Prospective study on the repercussions of low doses of remifentanil on sinoatrial function and in cardiac conduction and refractory period.].
Revista Brasileira de Anestesiologia 2007 October
BACKGROUND AND OBJECTIVES: Remifentanil is an opiod with fast onset of action and short acting, and its use in short-duration procedures has increased in the last few years. Bradycardia and asystole are among the side effects reported. The objective of this study was to evaluate the effects of this drug in cardiac conduction and refractory period in human beings.
METHODS: A prospective study with 16 patients, ages 18 to 65, both genders, ASA I to III, undergoing elective intracardiac electrophysiological study, was undertaken. Patients with disorders of the sinoatrial node and those with severe cardiac blocks were excluded. In the laboratory of electrophysiology, patients were sedated with midazolam (0.03 mg.kg-1) after 5 minutes the degree of sedation and degree of pain, systolic and diastolic blood pressure, heart rate and respiratory rate, and oxygen saturation were evaluated. The electrophysiologist evaluated cardiac conduction (duration of the QRS complex, and AA, AH, HV, and PA intervals), duration of sinoatrial node recovery, and cardiac refractory period (refractory period of the right atrium, right ventricle, and atrioventricular node). After the initial measurements, remifentanil was administered (bolus of 0.5 microg.kg-1 + infusion of 0.05 microg.kg-1.min-1) and, after 20 minutes, the same parameters were evaluated.
RESULTS: There was a reduction in systolic and diastolic blood pressure (p = 0.0001) between M0 and M1, and significant differences in respiratory rate and oxygen saturation, which were not statistically significant. The atrium-His interval (p = 0.006), recovery time of the sinoatrial node (p = 0.0004), refractory period of the right atrium (p = 0.001), and refractory period of the sinoatrial node (p = 0.0001) were all increased; however, there were no differences in heart rate between M0 and M1.
CONCLUSIONS: Remifentanil changes cardiac electrophysiological parameters and, in doses higher than the ones used in this study, can cause sinus bradycardia, asystole, and conduction defects.
METHODS: A prospective study with 16 patients, ages 18 to 65, both genders, ASA I to III, undergoing elective intracardiac electrophysiological study, was undertaken. Patients with disorders of the sinoatrial node and those with severe cardiac blocks were excluded. In the laboratory of electrophysiology, patients were sedated with midazolam (0.03 mg.kg-1) after 5 minutes the degree of sedation and degree of pain, systolic and diastolic blood pressure, heart rate and respiratory rate, and oxygen saturation were evaluated. The electrophysiologist evaluated cardiac conduction (duration of the QRS complex, and AA, AH, HV, and PA intervals), duration of sinoatrial node recovery, and cardiac refractory period (refractory period of the right atrium, right ventricle, and atrioventricular node). After the initial measurements, remifentanil was administered (bolus of 0.5 microg.kg-1 + infusion of 0.05 microg.kg-1.min-1) and, after 20 minutes, the same parameters were evaluated.
RESULTS: There was a reduction in systolic and diastolic blood pressure (p = 0.0001) between M0 and M1, and significant differences in respiratory rate and oxygen saturation, which were not statistically significant. The atrium-His interval (p = 0.006), recovery time of the sinoatrial node (p = 0.0004), refractory period of the right atrium (p = 0.001), and refractory period of the sinoatrial node (p = 0.0001) were all increased; however, there were no differences in heart rate between M0 and M1.
CONCLUSIONS: Remifentanil changes cardiac electrophysiological parameters and, in doses higher than the ones used in this study, can cause sinus bradycardia, asystole, and conduction defects.
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